ArticleAging cell2016
Alzheimer-related protein APL-1 modulates lifespan through heterochronic gene regulation in Caenorhabditis elegans.
Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
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- AI-Predicted mTOR Inhibitor Reduces Cancer Cell Proliferation and Extends the Lifespan ofInternational journal of molecular sciences · 2023Article
- CRISPR-activated expression of collagenmicroPublication biology · 2023Article
- SIN-3 functions through multi-protein interaction to regulate apoptosis, autophagy, and longevity in Caenorhabditis elegans.Scientific reports · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Sonneradon A Extends Lifespan ofMarine drugs · 2022Article
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- Lifespan-Associated Gene Expression Signatures of Recombinant BXD Mice ImplicatesFrontiers in genetics · 2021Article
- Succinate Dehydrogenase-Regulated Phosphoenolpyruvate Carboxykinase Sustains Copulation Fitness in Aging C. elegans Males.iScience · 2020Article
- Role of APP Interactions with Heterotrimeric G Proteins: Physiological Functions and Pathological Consequences.Frontiers in molecular neuroscience · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is an age-associated disease. Mutations in the amyloid precursor protein (APP) may be causative or protective of AD. The presence of two functionally redundant APP-like genes (APLP1/2) has made it difficult to unravel the biological function of APP during aging. The nematode Caenorhabditis elegans contains a single APP family member, apl-1. Here, we assessed the function of APL-1 on C. elegans' lifespan and found tissue-specific effects on lifespan by overexpression of APL-1. Overexpression of APL-1 in neurons causes lifespan reduction, whereas overexpression of APL-1 in the hypodermis causes lifespan extension by repressing the function of the heterochronic transcription factor LIN-14 to preserve youthfulness. APL-1 lifespan extension also requires signaling through the FOXO transcription factor DAF-16, heat-shock factor HSF-1, and vitamin D-like nuclear hormone receptor DAF-12. We propose that reinforcing APL-1 expression in the hypodermis preserves the regulation of heterochronic lin-14 gene network to improve maintenance of somatic tissues via DAF-16/FOXO and HSF-1 to promote healthy aging. Our work reveals a mechanistic link of how a conserved APP-related protein modulates aging.
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